A new analysis suggests that specific patterns of childhood hardship are linked to faster biological aging in women later in life. The research indicates that the impact of these early experiences varies depending on a person’s sex and racial or ethnic background. Published in the journal Psychoneuroendocrinology, the findings highlight how social disadvantages experienced decades ago may leave lasting chemical marks on our DNA.
Scientists have established that difficult childhood events can harm long-term health. These events are often called adverse childhood experiences, or ACEs. They include physical abuse, parental divorce, and household instability.
Researchers typically assess these hardships by counting them to create a cumulative score. A person who experienced divorce and poverty might get a score of two. However, this counting method has limitations.
It assumes that all difficult experiences affect the body in the same way. It also ignores how different problems often happen at the same time. A simple score might miss specific combinations of stressors that are particularly damaging.
A team of researchers led by Xiaoyan Zhang at New York University sought to correct this oversight. They used a statistical approach that looks for hidden patterns within data. This allowed them to group individuals based on the specific types of adversity they faced.
The study utilized data from the Health and Retirement Study. This is a large, long-running survey that represents the population of older adults in the United States. The analysis focused on 3,586 participants who provided blood samples in 2016.
From these blood samples, the researchers extracted DNA to analyze methylation. DNA methylation involves chemical tags that attach to the DNA molecule. These tags can turn genes on or off without changing the underlying genetic code.
Patterns of methylation change predictably as humans get older. This allows scientists to create “epigenetic clocks” that estimate a person’s biological age. If a person’s biological age is higher than their chronological age, they are aging at an accelerated rate.
The researchers used three advanced epigenetic clocks for their analysis. Two of them, known as GrimAge and PhenoAge, are designed to predict health risks and lifespan. The third, called DunedinPoAm, acts like a speedometer that measures how fast a person is aging at a specific moment.
Zhang and her colleagues aimed to view these biological markers through the lens of intersectionality. This theoretical framework suggests that race and sex are not separate categories. Instead, they represent interlocking systems that shape unique life experiences and health outcomes.
The team first identified distinct patterns of childhood adversity. They found that the patterns differed for Hispanic participants compared to Black and White participants. This required them to analyze the groups separately to ensure accuracy.
Among Black and White participants, the computer models identified two primary groups. The first was a “Low Adversity” class. The second was a “Financial Adversity” class, characterized by financial hardship and receiving financial help during childhood.
Among Hispanic participants, the models also found two distinct groups. One group was defined largely by “Parental Low Education.” The second group faced “Socioeconomic Adversity,” which included father’s unemployment and financial struggles in addition to low parental education.
The researchers then looked for connections between these groups and the epigenetic clocks. They found that women who grew up in the adversity classifications showed signs of faster biological aging. This connection was not statistically clear among the men in the study.
Black and White women in the Financial Adversity group had higher biological ages according to the GrimAge clock. They also showed a faster pace of aging on the DunedinPoAm speedometer. These results were compared against women in the Low Adversity group.
For Hispanic women, those in the Socioeconomic Adversity group tended to have higher biological ages on the PhenoAge clock. They also showed a faster pace of aging than Hispanic women in the Parental Low Education group. This suggests that the combination of financial instability and family disruption is particularly taxing on the body.
The study did not find these same patterns among men. Black and White men in the Financial Adversity group did not age significantly faster than those in the Low Adversity group. Similarly, Hispanic men did not show statistically meaningful differences based on their childhood adversity class.
However, the researchers observed that men generally exhibited faster biological aging than women across all groups. This aligns with broader medical data showing that men often have shorter lifespans and earlier onset of some age-related diseases. The lack of variation by adversity group suggests men might age biologically through different pathways.
The findings for women support the “weathering” hypothesis. This concept proposes that the chronic stress of social and economic disadvantage wears down the body’s systems over time. This cumulative burden eventually manifests as premature aging.
The connection between adversity and aging in women remained even after accounting for adult lifestyle factors. The researchers adjusted for variables such as smoking, body mass index, and adult poverty. Even with these adjustments, the link between early hardship and cellular aging persisted.
This suggests that early-life stress may be biologically embedded. The stress experienced during sensitive developmental periods appears to set a trajectory for health that lasts into older adulthood. It implies that interventions in adulthood might not fully reverse the effects of childhood disadvantage.
The researchers noted that GrimAge was the most consistent indicator of these differences. This particular clock was built using data on smoking and plasma proteins to predict mortality. Its sensitivity makes it a strong tool for detecting the long-term biological costs of stress.
There are important caveats to this research. The study relied on participants recalling their childhood experiences, which can be subject to memory errors. Additionally, the sample consisted of older adults who have survived to later life.
This focus on survivors means the study might miss individuals who died prematurely due to severe adversity. This survival bias could potentially weaken the observed associations. The results may also not apply to younger generations facing different types of modern stressors.
Future research is needed to understand why men and women respond differently to these early exposures. It is possible that biological differences in how sexes handle stress play a role. It is also possible that gendered social roles influence how trauma is internalized.
The authors suggest that future studies should look at younger populations. Tracking individuals over time would help confirm how these biological changes develop. Understanding the timing of these changes could reveal the best windows for intervention.
This study reinforces the idea that not all childhood adversity is the same. The specific combination of financial struggle and family instability matters. Furthermore, the biological impact of these experiences appears to be deeply intertwined with a person’s sex and background.
Addressing health disparities in older adults may require looking back to their earliest years. Policies that reduce child poverty and support family stability could have long-term benefits for healthy aging. The biological evidence suggests that social safety nets for children are also investments in public health.
The study, “Adverse childhood experiences patterns and biological aging in a representative sample of older Americans,” was authored by Xiaoyan Zhang, Natalie Slopen, Ariel A. Binns, and Adolfo G. Cuevas.
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